Fight Aging!

Age-related hearing loss is commonplace. It occurs due to loss of sensory hair cells in the inner ear, or due to the loss of axons connecting these cells to the brain. Evidence conflicts on which of these is the important mechanism. A good number of research programs aimed at reversing hearing loss are focused on generating more sensory hair cells, such as by reprogramming supporting cells of the inner ear to force transdifferentiation to the sensory hair cell fate. To the degree that new hair cells will forge new connections to the brain and correctly integrate into sensory processing circuits, this should fix both problems. Ensuring that this integration takes place sounds a more challenging than generating new hair cells, however.

Hearing loss correlates with a number of other aspects of aging, such as frailty, Alzheimer's disease, cognitive decline, and microstructural change in the brain. For brain aging one can at least consider that similar underlying mechanisms of neural and axonal damage are at work. For frailty, it is somewhat harder to guess at the shared cause. Similarly, researchers here note that the raised blood pressure of hypertension correlates with hearing loss, and once again it is not obvious as to where one should start looking for causation and shared mechanisms. Vascular damage is one of the evident consequences of hypertension, but it isn't clear as to how that interacts with sensory hair cells specifically.

Relationship Between Hypertension and Hearing Loss: Analysis of the Related Factors

This was a single-center population-based observational study, and clinical, biological, and hospital data were collected from the inpatient ward. In the present study, 517 patients (1034 ears) with or without hypertension were included, and the proportion of patients with hearing loss, mean pure-tone average hearing threshold, low-frequency pure-tone average hearing threshold (LFPTA), medium-frequency pure-tone average hearing threshold (MFPTA) and high-frequency pure-tone average hearing threshold (HFPTA) were evaluated. Risk factors related to hearing loss and hearing threshold were also estimated at different frequencies.

In this study, the hypertensive group exhibited more pronounced subclinical target organ damage and hearing impairment than the nonhypertensive group. Compared with the nonhypertensive group, the hypertensive group showed elevated albumin-to-creatinine ratio (ACR) levels, increased left ventricular mass index (LVMI) values, higher bilateral cardiovascular ankle index (CAVI) measurements, decreased bilateral ankle-brachial index (ABI) values, and a higher proportion of carotid intima-media thickening/plaque. Furthermore, the hypertension group demonstrated a higher prevalence of hearing loss at the mean pure-tone average hearing threshold and at individual frequencies.

Among these indicators, ABI and CAVI serve as markers of atherosclerosis and arterial stiffness, respectively, while ACR and LVMI indicate damage to the microvascular target organ in hypertension. These indicators have a significant clinical predictive value for subclinical target organ damage in hypertension. Therefore, the simultaneous appearance of hearing loss with these indicators may also be associated with early vascular damage caused by hypertension, which is consistent with previous studies. Although the exact mechanism underlying the influence of hypertension on the hearing threshold remains unclear, this study discovered that injuries to the vascular system can potentially contribute to hearing loss.